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Summary
Pulmonary edema is the accumulation of fluid in the lungs. The cause can be cardiogenic (e.g., acute myocardial infarction, congestive heart failure) or noncardiogenic (e.g., pneumonia, blood transfusion, preeclampsia, shock). Clinical features include progressive dyspnea and signs of hypoxemia (e.g., cyanosis, tachycardia). Cardiogenic pulmonary edema furthermore manifests with elevated jugular venous pressure and an S3 gallop on cardiac auscultation. Diagnosis and, especially, differentiation of causes involves laboratory studies, chest x-ray, and ECG as well as patient history and physical examination. Management involves oxygen supplementation and, depending on the cause, diuretics, morphine, and/or drugs to control blood pressure. Ventilatory support may be necessary in severe cases. Complications include acute respiratory distress syndrome (ARDS) and respiratory failure.
Classification
Types of pulmonary edema [2][3] | ||
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Cardiogenic pulmonary edema | Noncardiogenic pulmonary edema | |
Description |
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Pathophysiology |
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Etiology |
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Clinical features
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General symptoms
- Progressive dyspnea/tachypnea
- Signs of hypoxia (e.g., cyanosis, tachycardia)
- Cough, possibly with pink frothy sputum or expectoration
- Fever (secondary to pneumonia or sepsis)
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Physical examination findings [4]
- Rales or crackles on lung auscultation
- Increased tactile fremitus
- Dullness to percussion
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In cardiogenic edema:
- S3 gallop or murmurs on cardiac auscultation
- Elevated jugular venous pressure
- Peripheral edema
Diagnostics
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Laboratory studies
- CBC (increased in pneumonia or sepsis), serum electrolytes
- ↑ Cardiac biomarkers, such as troponin in patients with acute myocardial injury [3]
- ↑ BNP in patients with congestive heart failure
- Hypoalbuminemia (≤ 3.4 g/dL) in patients with acute decompensated heart failure
- Renal function tests (e.g., ↑ creatinine in renal failure)
- ↑ Lipase and/or amylase in patients with acute pancreatitis
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X-ray chest: posteroanterior and lateral views [5]
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Findings in cardiogenic pulmonary edema
- Central edema
- Kerley B lines: visible horizontal interlobular septa caused by pulmonary edema
- Pleural effusions
- Enlarged heart size
- Peribronchial cuffing
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Findings in noncardiogenic pulmonary edema
- Patchy and peripheral edema
- Possibly ground-glass opacities and consolidations with air bronchograms
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Findings in cardiogenic pulmonary edema
- ECG: to diagnose cardiac ischemia (e.g., myocardial infarction)
- Echocardiography: to diagnose or evaluate left ventricular systolic dysfunction and valvular dysfunction
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Pulmonary artery catheterization
- Gold standard to determine the cause of pulmonary edema
- Helps monitor systemic vascular resistance, cardiac output, filling pressures within the cardiac chambers, and pulmonary capillary wedge pressure (PCWP)
Management
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General
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To improve oxygenation
- Supplemental oxygenation
- Possibly, ventilatory support (invasive or noninvasive)
- Maintain adequate perfusion (e.g., IV fluid therapy) to prevent end-organ damage
- Treat the underlying disease
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To improve oxygenation
-
Medical treatment [6]
- Diuretics: treatment of choice (e.g., furosemide)
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Opioids (e.g., morphine)
- To reduce systemic vascular resistance (lowers blood pressure) and anxiety
- Used in pulmonary edema secondary to acute coronary syndrome
- Can cause respiratory depression and is, therefore, not generally recommended [7]
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IV nitroglycerin
- If systolic blood pressure is > 110 mm Hg
- Decreases preload and pulmonary congestion
- Nesiritide: to reduce PCWP and cardiac filling pressures
- Dobutamine or dopamine: to reduce pulmonary congestion in patients with low systolic blood pressure
- Nifedipine: in prophylaxis and treatment of high altitude pulmonary edema
Complications
- ARDS with progressive hypoxemia
- Respiratory failure, requiring mechanical ventilation
- Further complications depend on the underlying condition.
We list the most important complications. The selection is not exhaustive.
Flash pulmonary edema
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Description
- Sudden-onset, potentially life-threatening cardiogenic pulmonary edema that can cause acute hypoxemic respiratory failure
- Can occur in de novo heart failure and acute decompensated heart failure (ADHF)
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Risk factors [10]
- Long-standing poorly controlled hypertension [9]
- LVH and diastolic dysfunction
- Bilateral renal artery stenosis [11]
- Coronary artery disease
- Obstructive sleep apnea
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Triggers: similar to those of ADHF [10]
- Sympathetic activation: exertion, sympathomimetics (e.g., cocaine), medication nonadherence, psychosocial stress or anxiety [9]
- Abrupt hemodynamic changes
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Pathophysiology: Multiple processes lead to a vicious cycle of sympathetically-driven ↑ LVEDP and pulmonary edema. [9][10]
- Long-term hypertension → ↑ atherosclerosis and cardiac remodeling → ↑ afterload and ↑ MVO2, LVH, and ↑ diastolic dysfunction
- Sympathetic activation → peripheral and splanchnic vasoconstriction→ ↑ venous return and ↑ afterload → ↑ pulmonary edema and ↓ cardiac output
- ↑ Pulmonary edema and ↓ cardiac output → end-organ dysfunction and hypoxemia → ↑ sympathetic activation
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Clinical features [12]
- Hypertension, hypoxia
- Features of pulmonary congestion: e.g., crackles, signs of increased work of breathing, respiratory distress signs
- Minimal peripheral edema
- See also “Wet and warm” in “Classification of acute heart failure.”
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Diagnostics: similar to other types of pulmonary edema
- CXR: x-ray findings in pulmonary congestion
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Ultrasound
- B lines often present on lung ultrasound (See “POCUS in acute heart failure” for details)
- Echocardiography: See “Echocardiographic findings in AHF.”
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Management: See “Management of acute heart failure.”
- Stabilization with NIPPV and vasodilators for ADHF [10][12]
- Treatment of the underlying condition and trigger management.